Embodiments of the present disclosure generally relate to neurostimulation (NS), and more particularly to managing stimulation to block certain components of A-beta fibers, while stimulating other components of A-beta fibers within spinal cord structures.
Spinal cord stimulation (SCS) is used to treat a wide range of chronic neuropathic pain conditions by delivering electrical stimulation to select portions of the spinal cord. In the past, SCS therapy has been proposed in which a tonic therapy is defined by single pulses have a select pulse width, frequency and intensity. By way of example, tonic therapies have been proposed to manage cervical and lumbar pain. The pulse width, frequency and intensity may be changed, along with electrode configuration and placement on the spinal column in connection with pain relief for individual patients.
NS systems are devices that generate electrical pulses and deliver the pulses to nervous tissue to treat a variety of disorders. For example, spinal cord stimulation has been used to treat chronic and intractable pain. Another example is deep brain stimulation, which has been used to treat movement disorders such as Parkinson's disease and affective disorders such as depression. While a precise understanding of the interaction between the applied electrical energy and the nervous tissue is not fully appreciated, it is known that application of electrical pulses to certain regions or areas of nervous tissue can effectively reduce the number of pain signals that reach the brain. For example, applying electrical energy to the spinal cord associated with regions of the body afflicted with chronic pain can induce “paresthesia” (a subjective sensation of numbness or tingling) in the afflicted bodily regions.
SCS therapy, delivered via epidurally implanted electrodes, is a widely used treatment for chronic intractable neuropathic pain of different origins. Traditional tonic therapy evokes paresthesia covering painful areas of a patient. During SCS therapy calibration, the paresthesia is identified and localized to the painful areas by the patient in connection with determining correct electrode placement.
Recently, new stimulation configurations such as burst stimulation and high frequency stimulation, have been developed, in which closely spaced high frequency pulses are delivered to the spinal cord in a manner that does not generate paresthesias for the majority of patients, but still affords a therapeutic result. Neuropathic pain may result from lesions or diseases affecting the peripheral or central regions of the somatosensory system, and is difficult to treat. The first spinal cord stimulator as a treatment for neuropathic pain was implanted by Shealy in 1967, which was based on the gate-control theory proposed by Melzack and Wall (1965). The gate-control theory proposed that intrinsic activation of large diameter A-beta (Aβ) fibers blocks or inhibits the transmission of noxious stimuli to the brain via an inhibitory interneuron. It has been shown that electrical stimulation also may activate the large diameter A-beta fibers with the same result. The A-beta fibers transmit information from the peripheral nervous system through the dorsal root ganglion (DRG) before entering and projecting along the dorsal column.
Recent clinical evidence suggests that kilohertz frequency (˜10 kHz) spinal cord stimulation (KHFSCS) and burst spinal cord stimulation (SCS) can produce paresthesia-free analgesia (relief from pain). While evidence exists that KHFSCS or burst SCS provides an effective neuromodulation therapy for patients with chronic pain, little is known about the potential therapeutic mechanisms of action.
A need remains for methods and systems to manage neuromodulation therapy to produce paresthesia free analgesia.